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【Objective】 To investigate the effect of lentinan on Sorafenib resistance in hepatocellular carcinoma (HCC) cells BEL-7402/S and its mechanism. 【Methods】 CCK-8 method was used to detect the proliferation-toxicity of lentinan and Sorafenib on BEL-7402 and BEL-7402/S cells, and the drug resistance reversal multiple of Sorafenib. The effects of lentinan on mRNA and protein expressions of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF-1α) in BEL-7402/S cells were determined by RT-qPCR and Western blotting. 【Results】 Lentinan reduced the proliferation of BEL-7402 and BEL-7402/S cells. Lentinan showed at least a partial reversal of drug resistance to sorafenib in BEL-7402/S cells and down-regulated the mRNA and protein expressions of VEGF and HIF-1α in BEL-7402/S cells. 【Conclusion】 Lentinan can partially reverse the effect of BEL-7402/S cells on Sorafenib resistance, and the mechanism may be related to the down-regulation of VEGF and HIF-1α expressions.
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Objective To investigate the effect of rivaroxaban on HIF-α, P-selectin and TNF-αin patients with lower extremity venous thrombosis.Methods 41 cases from May 2014 to February 2015 were selected and randomly divided into two groups, 21 cases in the control group were treated by routine treatment, 20 cases in the experiment group were treated on the base of the control group with ivaroxaban.Serum HIF-α, P-selectin and TNF-αwere detected before and after the treatment.ResuIts Compared with the control group, the clinical effect were higher ( P0.05).HIF-α, P-selectin and TNF-αwere lower(P<0.05),HIF-αwas positively correlated with TNF-α(r =-0.468,P<0.05), and was not correlated with P-selectin, P-selectin was not associated with TNF-α.ConcIusion Rivaroxaban can effectively improve the lower limb venous thrombosis in patients with clinical symptoms, reduce serum HIF-α, P-selectin and TNF-αexpression, has better clinical curative effect, for clinical treatment of lower limb venous thrombosis has important significance.
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Objective To investigate the inhibitory effect of thalidomide on angiodysplasia.Methods Excisional intestinal specimens were collected and immunohistochemical examination was carried out.The human umbilical vein endothelial cells were cultured in vitro to exponential phase of growth,divided into six groups and synchronized for 24 hours.They were then stimulated with thalidomide (40-100 μg/ml) for 72 hours.MTT assay was used to assess cellular proliferation.ELISA,real-time quantitative PCB and western blot were applied to detect the expression of VEGF/HIF-1α of human umbilical vein endothelial cells (HUVEC).Results Immunohistochemical analysis of intestinal pathological specimens demonstrated higher expression of VEGF.ELISA showed that the expression of VEGF under hypoxia was obviously higher than that under normoxia [ ( 1199.3 ± 61.4) ng/L vs ( 864.7 ± 41.2 ) ng/L,P < 0.05 ].Real-time quantitative PCR and Western blot discovered that thalidomide inhibited the expression of VEGF/ HIF-1α of HUVEC (P < 0.05).The effect of thalidomide was dose-dependent.Conclusions Thalidomide can suppress the expression of HIF-1α and VEGF in HUVEC in vitro and then inhibit angiodysplasia,which may play a significant role in stopping the rebleeding in patients with recurrent gastrointestinal bleeding.